Open access peer-reviewed chapter
Abstract
Neurocysticercosis (NCC), a subtle parasite infection of the central nervous system, is a powerful example of the complex interaction between human behavior, zoonotic transmission, and neurological illness development. Given the disease’s worldwide prevalence and potentially fatal neurological consequences, research into NCC is critical for advancing knowledge, creating effective diagnostic tools and treatment options, and adopting preventative measures to lessen the disease’s impact. Cysticerci causes an immunological response in the CNS, resulting in inflammation and immune cell recruitment. The existence of intraventricular cysts, cysts in the cerebral aqueduct or fourth ventricle, and the degree of inflammation and scarring induced by the infection are all risk factors for the development of hydrocephalus. This book chapter provides an in-depth exploration of the pathology and pathogenesis of NCC, discussing the life cycle of the Taenia solium parasite, its invasion of the central nervous system, and the formation of cysticerci, as well as the diagnostic challenges and imaging findings, clinical manifestations, and potential neurological complications associated with NCC, serving as a valuable resource for medical professionals, researchers, and policymakers.
Keywords
- neuroimmunopathology
- neurocysticercosis
- zoonotic transmission
- neuropathology
- Taenia solium
1. Introduction
Neurocysticercosis (NCC), an insidious parasitic infection of the central nervous system, is a compelling testament to the intricate interplay between human behavior, zoonotic transmission, and neurological disorder pathogenesis. Caused by the larval stage of the pork tapeworm,
NCC is a complex parasitic infection that elicits diverse neuropathological changes within the central nervous system. The development of neuropathology in NCC follows a progressive course characterized by distinct stages. In the early vesicular stage, the cysticerci, comprising fluid-filled bladders housing the tapeworm larvae, exhibit a translucent membrane and contain a scolex with hooklets [5, 6]. As the infection progresses to the colloidal stage, degenerative changes occur, leading to a granulomatous reaction. This granuloma, composed of a necrotic core, edema, fibrous capsule, and inflammatory cells, contributes to the clinical manifestations commonly associated with NCC, such as seizures, headaches, and focal neurological deficits [6, 7]. Over time, some cysticerci may undergo calcification, resulting in the calcified stage where the parasites become inert, and the host response aims to contain the infection. Developing these neuropathological features in NCC underscores the dynamic interplay between the parasite, the host immune response, and the structural alterations within the central nervous system. Therefore, the evaluation and examination of neuropathological findings are very important [5, 6, 7].
NCC is paramount in infectious diseases and neurology due to its significant impact on public health and its potential to cause severe neurological complications. This parasitic infection, caused by the larval stage of the pork tapeworm,
Figure 1.
The proposed book chapter on NCC is necessary and of utmost importance in the medical and scientific community. NCC, caused by the larval stage of the pork tapeworm,
2. Inflammatory response in neurocysticercosis
Cysticerci triggers an immune response in the CNS, leading to inflammation and the recruitment of immune cells. The inflammatory response can vary depending on the location and stage of the cysticerci. Inflammatory cells, such as lymphocytes, macrophages, and eosinophils, infiltrate the cysticerci and the surrounding brain tissue, forming granulomas [10, 11, 12, 13, 14].
The relationship between the inflammatory response and neuropathology in NCC is complex and dynamic. The presence of the larval stage of the pork tapeworm,
2.1 Immune cell infiltration
The inflammatory response in NCC involves infiltrating various immune cells into the affected CNS tissue. These immune cells include lymphocytes, macrophages, eosinophils, and occasionally neutrophils. They are recruited to the site of infection in response to the presence of the larval cysticerci [11, 12, 13, 14].
2.2 Inflammatory mediators
Inflammatory mediators play a crucial role in NCC -associated inflammation. Cytokines, chemokines, and other inflammatory molecules are released by immune cells and contribute to the inflammatory response. These mediators include tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and interleukin-10 (IL-10), among others. They regulate immune cell activation, migration, and effector functions [11, 13, 14, 16].
3. Cysticerci formation
NCC is characterized by the formation of cysticerci, which are larval stages of the pork tapeworm,
3.1 Characteristics of cysticerci
Cysticerci are the larval stage of
3.1.1 Fluid-filled cysts
Cysticerci are bladder-like structures filled with clear or turbid fluid. The cysts vary in size, ranging from a few millimeters to several centimeters in diameter. Their size can influence the clinical presentation and potential complications [17, 18, 19].
3.1.2 Nodular stage
Over time, the cysticerci undergo a process of degeneration and transition into a nodular stage. In this stage, the cysts become more inflammatory and calcify, developing a thick fibrous capsule around the scolex. The nodular stage is associated with increased inflammatory response and clinical manifestations [3, 4, 18, 19].
3.1.3 Vesicular stage
In the early vesicular stage, the cysticerci are small and surrounded by a translucent membrane. These cysts are often asymptomatic and may go unnoticed. Histologically, the cysticerci in this stage are characterized by a thin eosinophilic membrane, a fluid-filled cavity, and a scolex (tapeworm’s head) with hooklets. Initially, the cysticerci are in a vesicular stage, characterized by a thin-walled cyst containing a small fluid-filled bladder with an invaginated scolex (tapeworm’s head). This stage is less inflammatory and may be asymptomatic [3, 4, 17, 18, 19].
In NCC, irregularly shaped large fluid cysts are a hallmark of NCC and are particularly common in areas of high endemicity. These cysts are typically spherical to oval in shape and vary in size, usually several centimeters in diameter. Their appearance in neuroimaging such as computed tomography (CT) or magnetic resonance imaging (MRI) is characterized by a well-defined, thin-walled, translucent structure filled with clear or slightly turbid fluid.
Cysts without scolex or protoscolex are also present. A distinctive feature of these cysts is the absence of a scolex or protoscolex within the cystic lümen [20, 21, 22]. Unlike other stages of cysticercosis where the scolex is identifiable and plays a critical role in attachment and growth, these large liquid cysts lack this vital structure. Although the cyst wall is thin, it can elicit an immune response in the host. Inflammation surrounding the cyst is a common feature and leads to the formation of a pericystic-enhancing edge on neuroimaging ([23, 24], Sotelo et al. 1985). This enhancing edge represents an inflammatory reaction to the presence of the cyst and is often used as a diagnostic criterion for NCC [21, 23, 25, 26, 27].
Large irregularly shaped liquid cysts are particularly common in hyperendemic areas of NCC, such as Mexico and Argentina [21, 24, 27]. The high prevalence in these regions is often attributed to factors such as pork consumption, sanitation, and cultural practices that influence the transmission of
Consequently, irregularly shaped large liquid cysts without scolex are a hallmark of NCC in hyperendemic areas. These cysts present unique challenges in diagnosis and treatment due to their potential to elicit inflammatory responses and neurological symptoms. Advanced imaging techniques and a deep understanding of the epidemiology of the disease are crucial to addressing this particular presentation of NCC in clinical practice and research in regions such as Mexico and Argentina.
3.1.4 Colloidal stage
As the cysticercus matures, it enters the colloidal stage. The cysticercus undergoes degenerative changes during this stage, leading to a granulomatous reaction around the parasite. The granuloma comprises a central necrotic area, surrounding edema, a fibrous capsule, and an outer layer of inflammatory cells. The colloidal stage is commonly associated with clinical symptoms such as seizures, headaches, and focal neurological deficits [4, 17, 18, 19].
3.1.5 Calcified stage
Over time, some cysticerci may undergo calcification, resulting in the calcified stage. Calcified lesions can be detected through neuroimaging studies like CT or MRI. Calcification represents a host response aimed at containing the infection. In the calcified stage, the cysticercus is no longer viable [3, 4, 18, 19].
4. Pathological features in neurocysticercosis
The pathological features of NCC depend on the infection’s stage and the cysticerci’s location within the central nervous system. The cysticerci reach the CNS through the bloodstream or lymphatic system. They can penetrate the blood-brain barrier and disseminate throughout the brain or spinal cord. The most common sites of cysticercosis formation in NCC include the brain parenchyma, ventricular system, subarachnoid space, and, rarely, the spinal cord [1, 14, 19, 28, 29, 30, 31].
4.1 Tissue damage
While the inflammatory response is aimed at controlling the infection, it can also contribute to tissue damage and neuropathology in NCC. The presence of immune cells and the release of inflammatory mediators can lead to the destruction of surrounding CNS tissue, disruption of the blood-brain barrier, and the release of toxic molecules. This tissue damage can result in clinical manifestations and neurological deficits [19, 28, 29, 31, 32].
4.2 Perilesional edema
Inflammation in NCC can lead to perilesional edema, the swelling of the tissue surrounding the cysticerci. Perilesional edema is attributed to increased vascular permeability, disrupted blood-brain barrier, and alterations in the balance of fluid regulation within the CNS. It can contribute to neurological symptoms and complications [14, 19, 28, 29, 31].
In some cases, NCC can lead to inflammation of the blood vessels in the brain, resulting in vasculitis. Vasculitis can cause disruption of the blood-brain barrier, leading to edema (swelling) and potentially causing neurological complications [19, 29, 31].
4.3 Neurological complications
The inflammatory response and associated neuropathology in NCC can lead to neurological complications. These complications may include seizures, focal neurological deficits, cognitive impairments, hydrocephalus, vasculitis, and increased intracranial pressure. Apart from these findings, meningoencephalitis and psychoses are among the common pathology [33]. The severity and extent of these complications depend on factors such as the number and location of cysticerci, the host’s immune response, and individual susceptibility [19, 28, 29, 31].
Understanding the relationship between the inflammatory response and neuropathology in NCC is crucial for comprehending the disease progression, developing therapeutic strategies, and managing neurological complications. The modulation of the inflammatory response and targeted interventions may hold promise for improving outcomes in NCC.
Spinal cysticercosis, although rare, can manifest as a cause of myelopathy, a neurological disorder affecting the spinal cord. The characteristic MRI features observed in affected individuals facilitate the recognition and accurate diagnosis of spinal cysticercosis. Therefore, clinicians must include spinal cysticercosis in the differential diagnosis when evaluating patients with myelopathy symptoms. In cases where spinal cysticercosis is confirmed, the recommended course of treatment involves the complete resection of the causative lesion and the administration of oral albendazole, an antiparasitic medication. This combined therapeutic approach has shown promising results, leading to the regression of symptoms in patients with spinal cysticercosis. Histopathological examination plays a crucial role in establishing the definitive diagnosis of spinal cysticercosis. By analyzing tissue samples obtained during surgical intervention, the characteristic features of the condition, such as the presence of parasitic larvae, can be identified. This histopathological confirmation not only confirms the diagnosis of spinal cysticercosis but also aids in differentiating it from other potential causes of spinal space-occupying lesions. In summary, recognizing spinal cysticercosis as a rare cause of myelopathy is aided by the characteristic MRI features observed in affected individuals. Clinicians should actively consider spinal cysticercosis during the differential diagnosis of myelopathy cases. When confirmed, complete resection of the causative lesion, coupled with oral albendazole administration, has demonstrated positive outcomes in symptom regression. Furthermore, the importance of histopathological examination cannot be understated, as it provides definitive confirmation of the diagnosis and aids in differentiating spinal cysticercosis from other spinal space-occupying lesions [34].
4.4 Granuloma formation and calcifications in neurocysticercosis
Granulomas are organized collections of immune cells that form in response to the presence of cysticerci. Granulomas typically consist of lymphocytes, macrophages, and multinucleated giant cells. The formation of granulomas is a host defense mechanism to contain and eliminate the parasite [15, 35, 36]. However, the inflammatory response can also contribute to tissue damage and neurological complications. As the cysticerci degenerate and the inflammatory response progresses, the cysts may be calcified [5, 15, 37]. Calcifications appear as dense, white areas in neuroimaging studies, such as computed tomography (CT) or magnetic resonance imaging (MRI). The presence of calcifications is an important diagnostic feature of NCC [5, 15, 35, 36, 37].
Granuloma formation is a prominent pathological feature in NCC, which occurs in response to the larval cysticerci of the pork tapeworm,
4.4.1 Granuloma formation in neurocysticercosis
Cellular composition: Granulomas in NCC are composed of various immune cells, including lymphocytes, macrophages, and multinucleated giant cells. Lymphocytes, particularly T cells, are involved in the initial recognition of the parasite and initiating the immune response. Macrophages play a crucial role in phagocytosing and destroying the cysticerci. Multinucleated giant cells, formed by the fusion of macrophages, are commonly observed in the granulomas and contribute to the destruction of the parasite [5, 15, 37].Cytokine and chemokine expression: The formation and maintenance of granulomas in NCC are regulated by the secretion of various cytokines and chemokines. Cytokines such as interferon-gamma, TNF-α, IL-1β, and IL-6 are produced by immune cells within the granuloma and play crucial roles in the modulation of the immune response. Chemokines, such as CCL2, CCL3, CCL4, and CCL5, are involved in the recruitment of immune cells to the site of infection [15, 35, 36].Fibrous capsule formation: Granulomas in NCC are characterized by the development of a fibrous capsule surrounding the cysticerci. The fibrous capsule is formed by depositing collagen and other extracellular matrix components. It serves as a physical barrier, preventing the parasite’s spread and reducing the surrounding tissue’s inflammatory response [5, 15, 37].Heterogeneity of granulomas: Granulomas in NCC can exhibit heterogeneity in their composition and organization. Some granulomas may be well-structured with a central core of necrotic debris surrounded by lymphocytes and macrophages. Others may have a less organized structure or show signs of degeneration. The heterogeneity of granulomas is thought to be influenced by factors such as the number and stage of the cysticerci, the host immune response, and the local microenvironment [15, 35, 36].
4.4.2 Calcifications in neurocysticercosis
Calcifications are a characteristic finding in neuroimaging studies of patients with NCC. They result from the degeneration and calcification of the larval cysticerci within the CNS [5, 7, 15, 35, 36, 37]. Calcifications in NCC appear as dense, white areas on neuroimaging studies such as CT scans. They are typically round or oval in shape and can vary in size, ranging from a few millimeters to several centimeters. Calcifications are commonly observed in the brain parenchyma, ventricles, subarachnoid space, and rarely, the spinal cord [5, 7, 37].
4.5 Hydrocephalus
Hydrocephalus is a common complication of NCC, particularly when cysts are located in the ventricular system or cause obstruction to the flow of cerebrospinal fluid (CSF). In certain instances, NCC can obstruct the flow of CSF within the brain, leading to hydrocephalus [38, 39, 40]. Hydrocephalus is characterized by an accumulation of CSF, causing increased intracranial pressure and enlargement of the ventricles. It can result from cysts’ obstruction of CSF pathways or inflammation-induced scarring [38, 39, 40, 41, 42].
4.5.1 Prevalence and risk factors
Hydrocephalus occurs in a significant proportion of NCC cases. The exact prevalence varies depending on geographic location and other factors, but studies have reported rates ranging from 7–35% [39, 40, 41]. Risk factors for the development of hydrocephalus include the presence of intraventricular cysts, cysts located in the cerebral aqueduct or fourth ventricle, and the degree of inflammation and scarring caused by the infection [39, 40, 41].
4.5.2 Mechanisms of hydrocephalus
Hydrocephalus in NCC can result from various mechanisms [38, 39, 40, 41, 42];
Obstructive hydrocephalus: One of the pivotal determinants of NCC-related neuropathologies is the size of the cysticerci within the central nervous system. Large cysts, when present, exert localized pressure on adjacent neural structures, leading to a spectrum of neurological deficits [20, 22, 24, 26]. This pressure effect can disrupt normal neuronal function, resulting in focal symptoms such as seizures, sensory deficits, and motor impairments. Moreover, the compression of blood vessels by these cysts may compromise cerebral perfusion, precipitating ischemic events and further exacerbating the clinical picture [20, 22, 24, 26].Aggregation of multiple cysts:
In certain instances, NCC takes on a more complex manifestation, characterized by the aggregation of multiple cysts into a single large bundle or cluster. This phenomenon intensifies the pressure effects within the confined intracranial space. The aggregative growth of cysticerci not only exacerbates focal neurological deficits but can also lead to increased intracranial pressure (ICP) [24, 43, 44, 45]. Elevated ICP is a grave concern, potentially giving rise to severe headaches, papilledema, and, in extreme cases, herniation syndromes. Timely intervention is imperative to alleviate these critical pressure-related consequences [24, 43, 44].
Cysts located in the ventricular system or causing obstruction to the flow of CSF can lead to obstructive hydrocephalus. The cysts physically block CSF flow, resulting in fluid accumulation and increased intracranial pressure. The obstruction can occur at the foramen of Monro, cerebral aqueduct, or fourth ventricle, depending on the location of the cysts [38, 39, 40, 41, 42].
Non-obstructive hydrocephalus: Inflammation and scarring induced by the infection can disrupt CSF’s normal absorption or impair the ventricular system’s flow dynamics. This can result in impaired CSF circulation and non-obstructive hydrocephalus [38, 39, 40, 41, 42].
Hydrocephalus associated with NCC can present with various symptoms depending on the severity and rapidity of CSF accumulation. Common clinical manifestations include headache, nausea, vomiting, papilledema (swelling of the optic disc), visual disturbances, gait disturbances, cognitive changes, and altered consciousness or coma in severe cases.
4.6 Obstruction of cerebrospinal fluid pathways
Another intriguing facet of NCC-related neuropathologies pertains to the obstruction of CSF pathways by cysticercal lesions. When cysts infiltrate the CSF circulation, they may impede the flow of this vital fluid, resulting in conditions such as hydrocephalus. The accumulation of CSF within the ventricular system can cause ventricular dilation and elevate ICP. Recognizing and addressing these obstructive patterns is crucial to preventing secondary complications associated with increased intracranial pressure [43, 45, 46, 47].
Neurocysticercosis exhibits an intricate interplay between its insidious onset and the subsequent emergence of neuropathological manifestations. While the initial stages of the disease may remain asymptomatic, the potential for neurological deficits becomes increasingly pronounced as the cysticerci grow and interact with their neural surroundings. Pressure effects arising from large cysts, the aggregation of multiple cysts, and the obstruction of cerebrospinal fluid pathways constitute critical determinants in the clinical trajectory of NCC. Early recognition, accurate diagnosis, and prompt management are imperative to mitigate the neurological sequelae associated with this parasitic infection.
5. Diagnosis
The diagnosis of hydrocephalus related to NCC involves a combination of clinical evaluation, neuroimaging, and CSF analysis. Neuroimaging studies, such as computed tomCT or MRI [48, 49, 50], are crucial in identifying the presence of hydrocephalus, assessing the location and extent of cysts, and evaluating the ventricular system. CSF analysis may rule out other causes of hydrocephalus and assess for signs of inflammation or infection [7, 39, 40, 41, 51].
The focus should be primarily on the laboratory diagnosis of NCC, an infectious disease affecting the nervous system and an important cause of epilepsy in developing countries. The primary immunodiagnostic approach involves assessing whether serological findings are compatible with the diagnosis suggested by imaging results. Lentil lectin-purified parasite antigens are used in enzyme-linked immunoelectrotransfer blot format to detect antibodies, while monoclonal antibody-based enzyme-linked immunosorbent assays (ELISAs) are used for antigen detection [52, 53]. The article also highlights recent developments in assay configurations that show promise in simultaneous antibody and antigen detection. However, it is important to note that the usefulness of immunodiagnostic tests is limited in areas endemic for NCC where confirmatory brain imaging may not be possible. This is because the tests available for immunodiagnosis will not significantly impact the clinical management of most individuals with asymptomatic or symptomatic NCC [9, 52, 53, 54].
6. Preventive measures
Neurocysticercosis is a significant public health concern globally, particularly in regions with poor sanitation and limited access to healthcare. The prevention of neurocysticercosis requires the implementation of effective preventive measures aimed at interrupting the transmission cycle and reducing the burden of the disease. By understanding and implementing these preventive measures, the incidence and impact of neurocysticercosis can be significantly mitigated, leading to improved public health outcomes and the alleviation of the socio-economic burden associated with this devastating parasitic infection [55, 56, 57].
6.1 Pig vaccination and anthelmintic medication to prevent T. solium cysticercosis infection
6.2 Updated pig management procedures to keep pigs away from human excrement
The transmission of
6.3 Inspection and adequate cooking of pigs to limit the danger of human infection
A thorough inspection and proper cooking of pork products play a pivotal role in preventing
6.4 Healthcare promoting hand cleanliness, food hygiene, sanitation, and pig management
A comprehensive healthcare approach plays a crucial role in preventing
Addressing the burden of
It is important to note that the management of hydrocephalus in NCC should be individualized, considering the patient’s clinical condition, the characteristics of the hydrocephalus, and the availability of resources and expertise. Close follow-up and multidisciplinary care involving neurologists, infectious disease specialists, and neurosurgeons are essential for optimal management of this complication.
These pathological features reflect the evolution and host response to NCC. The vesicular stage represents the early presence of viable cysticerci, while the colloidal stage shows an inflammatory response to degenerating parasites. The calcified stage indicates a resolved infection with inert, calcified lesions. Understanding these pathological features is crucial for diagnosing, managing, and treating NCC.
This section gave information about the pathology and pathogenesis of NCC. It is now recognized that irreversible pathologies occur with the appearance of neurological symptoms. At this stage, it is very important to understand the pathogenesis to develop treatment protocols. Each topic discussed in this chapter is important in understanding the disease.
In conclusion, this book chapter has provided an in-depth exploration of the pathology and pathogenesis of NCC, shedding light on the intricate mechanisms underlying this parasitic infection. Throughout the chapter, we have discussed the life cycle of the
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